title: Expression and function of colony-stimulating factors and their receptors in human prostate carcinoma cell lines.
abstract: BACKGROUND
  The predeliction for prostate carcinoma cells to metastasize to bone suggests the hypothesis that bone and/or bone marrow-derived factors may promote prostate carcinoma cell growth or survival, or serve as chemoattractants for these cells.
  
  
  METHODS
  We screened three prostate carcinoma cell lines, DU-145, PC-3, and LNCaP, for the expression of several hematopoiesis-associated colony-stimulating factors (CSFs) and their receptors using RT-PCR (reverse transcriptase-polymerase chain reaction) and immunohistochemical methods, and examined their functional effects.
  
  
  RESULTS
  All of these cell lines express granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF), and the DU-145 and PC-3 lines express stem-cell factor (SCF), as determined by RT-PCR and ELISA. Each of these cell lines expresses the receptors for SCF, GM-CSF, M-CSF, and granulocyte colony-stimulating factor (G-CSF). M-CSF enhanced the soft-agar clonogenicity of PC-3 and DU-145 cells, and GM-CSF stimulated all three cell lines. SCF stimulated the clonogenic growth of DU-145 cells. G-CSF marginally abrogated the induction of cell death in the PC-3 and LNCaP cell lines under serum-free conditions. GM-CSF and M-CSF stimulated modest chemotaxis of PC-3, DU-145, and LNCaP cells (most prominently in PC-3 cells).
  
  
  CONCLUSIONS
  These data suggest that 1) CSFs may be part of a network of paracrine and autocrine loops that modulate prostate carcinoma cell activity, and 2) the growth-stimulatory, survival-enhancing, and/or chemotactic actions of bone marrow-derived CSFs on prostate carcinoma cells may explain in part why bone is a preferential site of prostatic carcinoma metastases.
authors.affiliation: Cytokine/Cytokine Receptor Laboratory, LINK Laboratories, University of Massachusetts Medical Center, Worcester 01655, USA.
authors.forename: D M
authors.initials: DM
authors.lastname: Savarese
authors.forename: H
authors.initials: H
authors.lastname: Valinski
authors.forename: P
authors.initials: P
authors.lastname: Quesenberry
authors.forename: T
authors.initials: T
authors.lastname: Savarese
mesh_terms: D001483:Base Sequence; D002633:Chemotaxis / Q000502:physiology; D003115:Colony-Stimulating Factors / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D015972:Gene Expression Regulation, Neoplastic; D016179:Granulocyte Colony-Stimulating Factor / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D016173:Macrophage Colony-Stimulating Factor / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D008297:Male; D016133:Polymerase Chain Reaction / Q000379:methods; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D012333:RNA, Messenger / Q000032:analysis / Q000737:chemistry / Q000235:genetics; D016184:Receptors, Colony-Stimulating Factor / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology*; D019089:Stem Cell Factor / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D014407:Tumor Cells, Cultured
chemical_list: D003115:Colony-Stimulating Factors; D012333:RNA, Messenger; D016184:Receptors, Colony-Stimulating Factor; D019089:Stem Cell Factor; D016179:Granulocyte Colony-Stimulating Factor; D016173:Macrophage Colony-Stimulating Factor; D016178:Granulocyte-Macrophage Colony-Stimulating Factor